[Treatment of hypercalcemias].
Apart from the search for specific oncological treatments, interesting investigations are currently in progress into methods designed to increase bone resistance against tumoral aggression. Several substances are under study. Here the discussion will chiefly centre on the diphosphonates, their mechanism of action and indication in bone oncology. It has been seen that tumoral hypercalcemias (with or without bone metastases) essentially derive from disturbance of the balance between the huge mineral stores of the bone and the small extracellular space. It has also been learned that osteolysis inhibition is the major step in their treatment, while therapies designed to eliminate the calcium excess through the kidney (saline solutions, furosemide, ethacrinic acid, dialysis) or bind it with chelators (EDTA) can have only transitory effects. Tumoral osteolysis may be inhibited by drugs acting on bone and/or tumoral cells (mithramycin, calcitonin, corticosteroids etc.) or by the diphosphonates. At present the latter are the treatment of choice for tumoral hypercalcemias.
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D001859:Bone Neoplasms / Q000097:blood / Q000556:secondary*; D002116:Calcitonin / Q000627:therapeutic use; D004492:Edetic Acid / Q000627:therapeutic use; D004976:Ethacrynic Acid / Q000627:therapeutic use; D005665:Furosemide / Q000627:therapeutic use; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D006934:Hypercalcemia / Q000097:blood / Q000188:drug therapy*; D006435:Renal Dialysis; D012462:Saline Solution, Hypertonic
D000305:Adrenal Cortex Hormones; D012462:Saline Solution, Hypertonic; D005665:Furosemide; D002116:Calcitonin; D004492:Edetic Acid; D004976:Ethacrynic Acid
Traitement des hypercalcémies.